Cancer Cell International
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Primary researchExpression of platelet derived growth factor family members and the potential role of imatinib mesylate for cervical cancerLucia Taja-Chayeb1 , Alma Chavez-Blanco1 , Jorge Martínez-Tlahuel2 , Aurora González-Fierro1 , Myrna Candelaria2 , Jose Chanona-Vilchis3 , Elizabeth Robles2 and Alfonso Dueñas-Gonzalez1  1
Unidad de Investigación Biomédica en Cáncer, Instituto Nacional de Cancerología/Instituto de Investigaciones Biomédicas, UNAM, Mexico 2
Division of Clinical Research, Instituto Nacional de Cancerología, Mexico 3
Department of Pathology, Instituto Nacional de Cancerología, Mexico author email corresponding author email
Cancer Cell International 2006,
6:22doi:10.1186/1475-2867-6-22
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| Published: |
2 October 2006 |
Abstract
Background
Despite significant achievements in the treatment of cervical cancer, it is still a deadly disease; hence newer therapeutical modalities are needed. Preliminary investigations suggest that platelet-derived growth factor (PDGF) might have a role in the development of cervical cancer, therefore it is important to determine whether this growth factor pathway is functional and its targeting with imatinib mesylate leads to growth inhibition of cervical cancer cells.
Results
PDGF receptors (PDGFR) and their ligands are frequently expressed in cervical cancer and the majority exhibited a combination of family members co-expression. A number of intronic and exonic variations but no known mutations in the coding sequence of the PDGFRα gene were found in cancer cell lines and primary tumors. Growth assays demonstrated that PDGFBB induces growth stimulation that can be blocked by imatinib and that this tyrosine kinase inhibitor on its own inhibits cell growth. These effects were associated with the phosphorylation status of the receptor.
Conclusion
The PDGFR system may have a role in the pathogenesis of cervical cancer as their members are frequently expressed in this tumor and cervical cancer lines are growth inhibited by the PDGFR antagonist imatinib. |